Abstract
Pressure-passive perfusion beyond the upper limit of cerebral blood flow (CBF) autoregulation may be deleterious in patients with intracranial pathology. Therefore, monitoring of changes in CBF would be of clinical relevance in situations where clinical evaluation of adequate cerebral perfusion is impossible. Noninvasive monitoring of cerebral blood flow velocity using transcranial Doppler sonography (TCD) may reflect relative changes in CBF. This study correlates the effects of angiotensininduced arterial hypertension on CBF and cerebral blood flow velocity in dogs. Heart rate (HR) was recorded using standard ECG. Catheters were placed in both femoral arteries and veins for measurements of mean arterial blood pressure (MAP), blood sampling and drug administration. A left ventricular catheter was placed for injection of microspheres. Cerebral blood flow velocity was measured in the basilar artery through a cranial window using a pulsed 8 MHz transcranial Doppler ultrasound system. CBF was measured using colour-labelled microspheres. Intracranial pressure (ICP) was measured using an epidural probe. Arterial blood gases, arterial pH and body temperature were maintained constant over time. Two baseline measures of HR, MAP, CBF, cerebral blood flow velocity and ICP were made in all dogs (n = 10) using etomidate infusion (1.5 mg · kg−1 · hr−1) and 70% N2O in O2 as background anaesthesia. Following baseline measurements, a bolus of 1.25 mg angiotensin was injected iv and all variables were recorded five minutes after the injection. Mean arterial blood pressure was increased by 76%. Heart rate and ICP did not change. Changes in MAP were associated with increases in cortical CBF (78%), brainstem CBF (87%) and cerebellum CBF(64%). Systolic flow velocity increased by 27% and Vmean increased by 31% during hypertension (P < 0.05). Relative changes in CBF and blood flow velocity were correlated (CBF cortex — Vsyst: r = 0.94, CBF cortex — Vmean: r = 0.77; P < 0.001; CBF brainstem — Vsyst: r = 0.82, CBF brainstem — Vmean: r = 0.69; P < 0.05). Our results show that increases in arterial blood pressure beyond the upper limit of cerebral autoregulation increase CBF in dogs during etomidate and N2O anaesthesia. The changes in CBF are correlated with increases in basilar artery blood flow velocity. These data suggest that TCD indicates the upper limit of the cerebral autoregulatory response during arterial hypertension. However, the amount of CBF change may be underestimated with the TCD technique.
Résumé
La pression passive de perfusion cérébrale au-dessus du seuil supérieur de l’autorégulation du débit sanguin cérébral (CBF) peut être fatale chez des patients atteints de pathologie intracrânienne. Ainsi le monitorage du changement du CBF sera important dans les cas où l’évaluation clinique d’une perfusion cérébrale adéquate n’est pas possible. Le monitorage de la vélocité du flot sanguin cérébral par un doppler transcrânien peut refléter des changements relatifs du CBF. Cette étude met en corrélation les effets de l’hypertension artérielle provoqués par l’angiotensine sur le flot sanguin cérébral local (rCBF) et la vélocité du débit sanguin cérébral chez des chiens. La fréquence cardiaque a été enregistrée en continu (ECG). Pour mesurer la pression artérielle moyenne (MAP), pour les prélèvements sanguins et l’administration des médicaments, des cathéters ont été placés dans les artères et veines fémorales. Pour une injection des microsphères, un cathéter a été placé dans le ventricule gauche. La vélocité du flot sanguin cérébral a été mesurée au niveau du tronc basilaire par une fenêtre osseuse en utilisant un doppler transcrânien puisé 8 MHz (TCD). CBF a été mesuré en utilisant des microsphères colorées. La pression intracrânienne (ICP) a été mésurée par sonde épidurale. Les gaz sanguins artériels, le pH artériel et la température corporelle ont été maintenus constants pendant toute la durée du protocole. Deux mesures de contrôle de tous les paramètres MAP, HR, CBF, de la vélocité du flot sanguin et ICP ont été enregistrées chez tous les chiens (n = 10) anesthésiés par l’infusion d’étomidate (1,5 mg · kg−1 · hr−1) et au protoxyde d’azote (70%) dans l’oxygène. Après ces mesures de contrôle, un bolus d’angiotensine 1,25 mg a été injecté et tous les paramètres ont été enregistrés cinq minutes après l’injection. MAP a augmenté de 76%. La fréquence cardiaque et la pression intracrânien n’ont pas changé. Les changements de la pression artérielle moyenne ont été associés aux changements significatifs du CBF cortical (78%), du CBF du tronc cérébral (87%) et du CBF du cervelet (64%). Pendant la durée de l’hypertension, Vsyst a augmenté de 27% et Vmoyenne de 31% (P < 0,05). Il y a eu une corrélation entre les changements relatifs du CBF et la vélocité du débit sanguin cérébral (CBF cortex — Vsyst: r = 0,94, CBF cortex — Vmoyenne: r = 0,77; P < 0,001; CBF tronc cérébral — Vsyst: r = 0,52, CBF tronc cérébral — Vmoyenne: r = 0,69; P < 0,05). Nos résultats montrent que chez des chiens anesthésiés au proloxyde d’azote et à l’étomidate, les augmentations de la pression artérielle au-dessus de la limite supérieure de l’autorégulation cérébrale augmentent le flot sanguin cérébral global et régional. Il y a une corrélation entre les changements du CBF et les augmentations de la vélocité du flot sanguin du tronc basilaire. Ces données suggèrent que TCD indique la limite supérieure de l’autorégulation cérébrale pendant la durée de l’hypertension artérielle. Cependant, le taux du changement du CBF peut être sous-estimé par la technique du TCD.
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References
Rapela CE, Green HD. Autoregulation of canine cerebral blood flow. Circ Res 1964; 14 (Suppl 1): 205–11.
Busija DW, Heistad DD. Factors involved in the physiological regulation of the cerebral circulation. Rev Physiol Biochem Pharmacol 1984; 101: 161–211.
Werner C, Hoffman WE, Kochs E, Albrecht RD, Schulte am Esch J. The effects of propofol on cerebral blood flow in correlation to cerebral blood flow velocity in dogs. Journal of Neurosurgical Anesthesia 1992; 4: 41–6.
Werner C, Hoffman WE, Baughman VL, Albrecht RF, Schulte am Esch J. Effects of sufentanil on cerebral blood flow, cerebral blood flow velocity, and metabolism in dogs. Anesth Analg 1991; 72: 177–81.
Pilato MA, Bissonnette B, Lerman J. Transcranial Doppler: response of cerebral blood-flow velocity to carbon dioxide in anaesthetized children. Can J Anaesth 1991; 38: 37–42.
Van der Linden JA, von Ahn H, Ekroth R, Tydén H. Middle cerebral artery blood flow velocity during coronary surgery; influences of clinical variables. J Clin Anesth 1990; 2: 7–15.
Hale SL, Alker KJ, Kloner RA. Evaluation of nonradioactive, colored microspheres for measurement of regional myocardial blood flow in dogs. Circulation 1988; 78: 428–34.
Hoffman WE, Werner C, Kochs E, Segil L, Edelman G, Albrecht RF. Cerebral and spinal cord blood flow in awake and fentanyl/N2O anesthetized rats: evidence for preservation of blood flow autoregulation during anesthesia. Journal of Neurosurgical Anesthesia 1992; 4: 31–5.
Sokrab TE, Johansson BB. Regional cerebral blood flow in acute hypertension induced by adrenaline, noradrenaline and phenylephrine in the conscious rat. Acta Physiol Scand 1989; 137: 101–6.
Hernandez MJ, Brennan RW, Bowman GS Cerebral blood flow autoregulation in the rat. Stroke 1978; 9: 150–4.
MacKenzie ET, Strandgaard S, Graham DI, Jones JV, Harper AM, Farrar JK. Effects of acutely induced hypertension in cats on pial arteriolar caliber, local cerebral blood flow, and the blood-brain barrier. Circ Res 1976; 39: 33–41.
Kontos HA, Wei EP, Navari RM, Levasseur JE, Rosenblum WI, Patterson JL Jr. Responses of cerebral arteries and arterioles to acute hypotension and hypertension. Am J Physiol 1978; 234: H371–83.
Edvinsson L, Hardebo J-E, Owman C. Effects of angiotensin II on cerebral blood vessels. Acta Physiol Scand 1979; 105: 381–3.
Wei EP, Kontos HA, Patterson JL Jr. Vasoconstrictor effect of angiotensin on pial arteries. Stroke 1978; 9: 487–9.
Joyner WL, Young R, Blank D, Ecclestone-Joyner CA, Gilmore JP. In vivo microscopy of the cerebral microcirculation using neonatal allografts in hamsters. Circ Res 1988; 63: 758–66.
Patel PM, Mutch WAC. The cerebral pressure-flow relationship during 1.0 MAC isoflurane anesthesia in the rabbit: the effect of different vasopressors. Anesthesiology 1990; 72: 118–24.
Haberl RL, Decker PJ, Einhäupl KM. Angiotensin degradation products mediate endothelium-dependent dilation of rabbit brain arterioles. Circ Res 1991; 68: 1621–7.
Haberl RL, Anneser F, Villringer A, Einhäupl KM. Angiotensin II induces endothelium-dependent vasodilatation of rat cerebral arterioles. Am J Physiol 1990; 258: H1840–6.
Aaslid R. Transcranial Doppler Sonography. Wien, New York: Springer Verlag, 1986.
Giulioni M, Ursino M, Alvisi C. Correlations among intracranial pulsatility, intracranial hemodynamics, and transcranial Doppler wave form: literature review and hypothesis for future studies. Neurosurgery 1988; 22: 807–12.
Klingelhöfer J, Conrad B, Benecke R, Sander D, Markakis E. Evaluation of intracranial pressure from transcranial Doppler studies in cerebral disease. J Neurol 1988; 235: 159–62.
Dewey RC, Pieper HP, Hunt WE. Experimental cerebral hemodynamics — vasomotor tone, critical closing pressure, and vascular bed resistance. J Neurosurg 1974; 41: 597–606.
Kochs E, Schulte am Esch J. Somatosensory evoked responses during and after graded brain ischemia in goats. Eur J Anaesthesiol 1991; 8: 257–65.
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Werner, C., Kochs, E., Hoffman, W.E. et al. Cerebral blood flow and cerebral blood flow velocity during angiotensin-induced arterial hypertension in dogs. Can J Anaesth 40, 755–760 (1993). https://doi.org/10.1007/BF03009772
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DOI: https://doi.org/10.1007/BF03009772